脑精素注射液治疗脑功能障碍患者900例临床疗效观察

目的观察脑精素注射液治疗脑功能障碍的临床效果。方法分别对脑精素治疗进行疗效观察。结果脑梗死组患者自觉症状有好转 ,体征明显改善 ,总有效率为 89.1%、脑出血组患者症状完全消失 ,总有效率为96.7%。结论脑精素作为小分子多肽类生化制剂 。

脑精素的研制及其临床疗效观察

目的:研究脑精素的制备工艺以及脑精素治疗脑功能障碍900例疗效分析。方法:从脑精素制备工艺、质量标准、疗效观察三方面进行研究。结果和结论:脑精素作为小分子多肽类生化制剂,治疗脑功能障碍患者总有效率88.1％。

脑精素注射液细菌内毒素检查法的研究

目的:建立脑精素注射液的细菌内毒素检查法。方法:根据中国药典2000年版二部收载的细菌内毒素检查法的要求进行实验。结果:将脑精素注射液稀释30倍,以标示灵敏度为0.5EU·mL^(-1)的鲎试剂检查是有效的。结论:鲎试验法取代家兔法对脑精素注射液进行热原检查是可行的。

Effect of AVP on brain edema following traumatic brain injury

Objective： To evaluate plasma arginine vasopressin （AVP） level in patients with traumatic brain injury and investigate the role of AVP in the process of brain edema. Methods ： A total of 30 patients with traumatic brain injury were involved in our study. They were divided into two groups by Glasgow Coma Scale： severe tranmatic brain injury group （ STBI, GCS ≤ 8 ） and moderate traumatic brain injury group （ MTBI, GCS 〉 8 ）. Samples of venous blood were collected in the morning at rest from 15 healthy volunteers （control group）and within 24 h after traumatic brain injury from these patients for AVP determinations by radioimmunoassay. The severity and duration of the brain edema were estimated by head CT scan. Results： plasma AVP levels （ng/L） were （mean± SD） control, 3.06 ± 1.49; MTBI, 38. 12 ± 7. 25; andSTBI, 66. 61 ± 17. 10. The plasma level of AVP was significantly increased within 24 h after traumatic brain injury and followed by the reduction of GCS, suggesting the deterioration of cerebral injury （ P 〈 0.01 ）. And the AVP level was correlated with the severity （ STBI r = 0. 919, P 〈 0.01 ; MTBI r = 0. 724, P 〈 0.01 ） and the duration of brain edema （STBI r =0.790, P 〈0.01; MTBI r =0.712, P〈0.01）. Conclusions. The plasma AVP level is dosely associated with the severity of traumatic brain injury. AVP may play an important role in pathogenesis of brain edema after traumatic brain injury.

Early changes of arginine vasopressin and angiotensin II in patients with acute cerebral injury

Objective: To study the changes and clinical significance of arginine vasopressin (AVP) and angiotensin II (AT II) in patients with acute moderate and severe cerebral injury. Methods: The early plasma concentration was checked by radioimmunoassay in 47 cases of acute moderate and severe cerebral injury, 30 cases of non cerebral injury and 30 healthy volunteers. Results: The early plasma concentrations of AVP ( 50.23 ng/L± 15.31 ng/L) and AT II ( 248.18 ng/L± 82.47 ng/L) in cerebral injury group were higher than those in non cerebral injury group (AVP for 30.91 ng/L± 11.48 ng/L and AT II for 120.67 ng/L± 42.49 ng/L, P< 0.01 ). The early plasma concentrations of AVP and AT II in cerebral injury group were also obviously higher than those of the volunteers (AVP for 5.16 ng/L± 4.23 ng/L and AT II for 43.11 ng/L± 16.39 ng/L, P< 0.001 ). At the same time, the early plasma level of AVP ( 58.90 ng/L± 18.12 ng/L) and AT II ( 292.13 ng/L± 101.17 ng/L) was higher in severe cerebral injured patients than moderate cerebral injured ones (AVP for 36.68 ng/L± 12.16 ng/L and AT II for 201.42 ng/L± 66.10 ng/L, P< 0.01 ). The early level of AVP and AT II was negatively related to the GCS scales in acute cerebral injury. The early plasma concentrations of AVP ( 45.98 ng/L± 13.48 ng/L) and AT II ( 263.28 ng/L± 80.23 ng/L) were lower in epidural hematoma group than those of subdural hematoma and cerebral injury group (AVP for 64.12 ng/L± 15.56 ng/L and AT II for 319.82 ng/L± 108.11 ng/L, P< 0.01 ). Conclusions: AVP and AT II may play an important role in pathophysiologic process in the secondary cerebral injury. The more severe the cerebral injury is, the higher the early level of AVP and AT II will be. The early plasma level of AVP and AT II may be one of the severity indexes of cerebral injury.